Cell-mediated autoimmunity, particularly that involving autoreactive T cells, participates in mediating anti-glomerular basement membrane(GBM) disease. However, direct kidney injury mediated by renal infiltrated T cel...Cell-mediated autoimmunity, particularly that involving autoreactive T cells, participates in mediating anti-glomerular basement membrane(GBM) disease. However, direct kidney injury mediated by renal infiltrated T cells has not been clearly elucidated in humans. The T cell profile(CD3, CD4, CD8, IL-17, and foxp3) and macrophage(CD68) were examined by immunohistochemistry on renal biopsy tissues from 13 patients with anti-GBM disease. The correlation between cell infiltration and clinical data was also analyzed. We found that the distribution of T cell infiltration was predominant in the peri-glomerular and interstitial areas. CD3^+ T cell infiltratrion around the glomeruli with cellular crescent formations was significantly higher than that around the glomeruli with mild mesangial proliferation. CD8^+ T cells significantly accumulated around the glomeruli with cellular crescents without Ig G deposits compared to those with Ig G deposits. The prevalence of infiltrating CD8^+ T cells was correlated with the percentage of ruptured Bowman's capsules. In conclusion, cellular immunity may play a crucial role in the inflammatory kidney injury in anti-GBM patients. The periglomerular infiltration of T cells, especially CD8^+ T cells, may participate in the pathogenic mechanism of glomerular damage.展开更多
基金supported by the National Basic Research Program of China (2012CB517702)the Natural Science Foundation of China (81321064,81330020, 81370801, 81400703)
文摘Cell-mediated autoimmunity, particularly that involving autoreactive T cells, participates in mediating anti-glomerular basement membrane(GBM) disease. However, direct kidney injury mediated by renal infiltrated T cells has not been clearly elucidated in humans. The T cell profile(CD3, CD4, CD8, IL-17, and foxp3) and macrophage(CD68) were examined by immunohistochemistry on renal biopsy tissues from 13 patients with anti-GBM disease. The correlation between cell infiltration and clinical data was also analyzed. We found that the distribution of T cell infiltration was predominant in the peri-glomerular and interstitial areas. CD3^+ T cell infiltratrion around the glomeruli with cellular crescent formations was significantly higher than that around the glomeruli with mild mesangial proliferation. CD8^+ T cells significantly accumulated around the glomeruli with cellular crescents without Ig G deposits compared to those with Ig G deposits. The prevalence of infiltrating CD8^+ T cells was correlated with the percentage of ruptured Bowman's capsules. In conclusion, cellular immunity may play a crucial role in the inflammatory kidney injury in anti-GBM patients. The periglomerular infiltration of T cells, especially CD8^+ T cells, may participate in the pathogenic mechanism of glomerular damage.
